Cyclic ADP‐ribose does not affect cardiac or skeletal muscle ryanodine receptors

FEBS Letters

Louis, Charles F.¹  Fruen, Bradley R.¹  Velez, Patricio²  Shomer, Nirah H.¹  Mickelson, James R.¹ 

[1] Department of Veterinary PathoBiology, University of Minnesota, 1988 Fitch Ave., Rm 295, St. Paul, MN 55108, USA;Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston, TX 77550, USA

关键词: Cyclic ADP-ribose;    Ryanodine receptor;    Ca2+ release channel;    Sarcoplasmic reticulum;   

DOI  :  10.1016/0014-5793(94)00931-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The cardiac muscle isoform of the ryanodine receptor/Ca²⁺ release channel (RYR) has been proposed to be an important target of cyclic ADP-ribose (cADPR) action in mammalian cells. However, we now demonstrate that neither cADPR (0.1–5 μM), nor the related metabolites, β-NAD⁺ (0.1–30 mM) and ADP-ribose (0.1–5 μM), affected cardiac RYR activity as determined by [³H]ryanodine binding to cardiac sarcoplasmic reticulum (SR) vesicles. Similarly, cADPR (1 μM) failed to activate single cardiac RYR channels in planar lipid bilayers. Skeletal muscle SR [³H]ryanodine binding was also unaffected by cADPR (up to 30 μM). These results argue against a direct role for the well-characterized RYRs of cardiac or skeletal muscle in mediating cADPR-activated Ca²⁺ release.

【 授权许可】

Unknown